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il 1β inhibitor ilaris canakinumab  (Novartis)

 
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    Novartis il 1β inhibitor ilaris canakinumab
    Il 1β Inhibitor Ilaris Canakinumab, supplied by Novartis, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/canakinumab/1%CE%B2+canakinumab+il+ilaris+inhibitor/pmc12694644-752-1-0
    Average 86 stars, based on 1 article reviews
    il 1β inhibitor ilaris canakinumab - by Bioz Stars, 2026-09
    86/100 stars

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    Blocking Assay:

    Article Title: The NLRP3 Inflammasome: Mechanisms of Activation, Regulation, and Therapeutic Opportunities
    Article Snippet: Canakinumab (Novartis) , IL‐1β neutralizing monoclonal antibody , CAPS , NCT01276522 , III , ∼60 , Sustained efficacy in Schnitzler's syndrome , Approved.

    Article Title: The NLRP3 Inflammasome: Mechanisms of Activation, Regulation, and Therapeutic Opportunities
    Article Snippet: Canakinumab (Novartis) , IL‐1β neutralizing monoclonal antibody , AS , NCT01327846 , II , 10061 , Lower rate of recurrent cardiovascular events independent of lipid‐lowering , Completed.

    Article Title: The NLRP3 Inflammasome: Mechanisms of Activation, Regulation, and Therapeutic Opportunities
    Article Snippet: Canakinumab (Novartis) , IL‐1β neutralizing monoclonal antibody , CAPS , NCT01105507 , I , — , Confirmed safety and efficacy in CAPS patients , Completed.

    Article Title: The NLRP3 Inflammasome: Mechanisms of Activation, Regulation, and Therapeutic Opportunities
    Article Snippet: Canakinumab (Novartis) , IL‐1β neutralizing monoclonal antibody , FCAS , NCT00991146 , I/II , — , Safety and efficacy confirmed , Completed.

    Article Title: The NLRP3 Inflammasome: Mechanisms of Activation, Regulation, and Therapeutic Opportunities
    Article Snippet: Canakinumab (Novartis) , IL‐1β neutralizing monoclonal antibody , FCAS , NCT00487708 , I , — , Safety and efficacy confirmed , Completed.

    Article Title: Interleukin-17 family in health and immune diseases: From origin to clinical implications
    Article Snippet: Canakinumab , IL-1β , May. 2019, FDA approved , Novartis , SJIA, CAPS.

    Article Title: The NLRP3 Inflammasome: Mechanisms of Activation, Regulation, and Therapeutic Opportunities
    Article Snippet: Canakinumab (Novartis) , IL‐1β neutralizing monoclonal antibody , FCAS , NCT01302860 , II/III , — , Safety and efficacy confirmed , Completed.

    Cell Differentiation:

    Article Title: The NLRP3 Inflammasome: Mechanisms of Activation, Regulation, and Therapeutic Opportunities
    Article Snippet: Canakinumab (Novartis) , IL‐1β neutralizing monoclonal antibody , CAPS , NCT01276522 , III , ∼60 , Sustained efficacy in Schnitzler's syndrome , Approved.

    Article Title: The NLRP3 Inflammasome: Mechanisms of Activation, Regulation, and Therapeutic Opportunities
    Article Snippet: Canakinumab (Novartis) , IL‐1β neutralizing monoclonal antibody , AS , NCT01327846 , II , 10061 , Lower rate of recurrent cardiovascular events independent of lipid‐lowering , Completed.

    Article Title: The NLRP3 Inflammasome: Mechanisms of Activation, Regulation, and Therapeutic Opportunities
    Article Snippet: Canakinumab (Novartis) , IL‐1β neutralizing monoclonal antibody , CAPS , NCT01105507 , I , — , Confirmed safety and efficacy in CAPS patients , Completed.

    Article Title: The NLRP3 Inflammasome: Mechanisms of Activation, Regulation, and Therapeutic Opportunities
    Article Snippet: Canakinumab (Novartis) , IL‐1β neutralizing monoclonal antibody , FCAS , NCT00991146 , I/II , — , Safety and efficacy confirmed , Completed.

    Article Title: The NLRP3 Inflammasome: Mechanisms of Activation, Regulation, and Therapeutic Opportunities
    Article Snippet: Canakinumab (Novartis) , IL‐1β neutralizing monoclonal antibody , FCAS , NCT00487708 , I , — , Safety and efficacy confirmed , Completed.

    Article Title: Interleukin-17 family in health and immune diseases: From origin to clinical implications
    Article Snippet: Canakinumab , IL-1β , May. 2019, FDA approved , Novartis , SJIA, CAPS.

    Article Title: The NLRP3 Inflammasome: Mechanisms of Activation, Regulation, and Therapeutic Opportunities
    Article Snippet: Canakinumab (Novartis) , IL‐1β neutralizing monoclonal antibody , FCAS , NCT01302860 , II/III , — , Safety and efficacy confirmed , Completed.



    Similar Products

    il 1β inhibitor ilaris canakinumab  (Novartis)
    86
    Novartis il 1β inhibitor ilaris canakinumab
    Il 1β Inhibitor Ilaris Canakinumab, supplied by Novartis, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/canakinumab/1%CE%B2+canakinumab+il+ilaris+inhibitor/pmc12694644-752-1-0
    Average 86 stars, based on 1 article reviews
    il 1β inhibitor ilaris canakinumab - by Bioz Stars, 2026-09
    86/100 stars
    		  Buy from Supplier
    canakinumab  (Novartis)
    86
    Novartis canakinumab
    Blocking mechanisms of interleukin-17 signaling in immune diseases. The addition of IL-6 + TGF-β or IL-6 + IL-1β + IL-23 to naïve mouse CD4 + T cells is required for T cells to upregulate RORγt and produce Th17 cytokines. IL-17 signaling can be achieved by blocking interleukin-17A (Secukinumab, Lxekizumab, and Nanakimab) and interleukin-17F (Bimekizumab) antibodies. IL-6 and TGF-β secreted by B cells are important inducers of Th17 cells. Antibodies targeting CD20 (Rituximab, Ofatumumab, Obinutuzumab, or Ocrelizumab) and CD19 (Inebilizumab) can lead to B-cell exhaustion and indirectly hinder the differentiation of Th17 cells. Inhibitors of IL-6R (Satralizumab), IL-1β <t>(Canakinumab)</t> or IL-23 (Uselkumab, Tildrakizumab, and Risankizumab), which indirectly target the IL-17 signaling pathway, can also affect Th17 cell differentiation. Blocking the infiltration of immune cells into the CNS can prevent autoimmune neuroinflammation. Natalizumab is an approved monoclonal antibody designed to specifically hinder this process by targeting VLA4/VCAM1, an integrin expressed on almost all immune cell subsets. DICAM and Integrin α3 are characteristically expressed on Th17 cells and bind to αvβ3 integrin and Laminin α5 on the blood‒brain barrier, respectively. Anti-DICAM and anti-αvβ3 integrin antibodies reduced the number of Th17 cells in the CNS. Created with BioRender.com. CD19: Cluster of differentiation 19; CD20: Cluster of differentiation 20; DICAM: dual immunoglobulin domain containing cell adhesion molecule; IL-1β: interleukin-1β; IL-6: interleukin-6; IL-17: interleukin-17; IL-17A: interleukin-17A; IL-17F: interleukin-17F; IL-17R: interleukin-17 receptor; IL-23: interleukin-23; TGF-β: tumor growth factor-β; Th0: helper T-cell 0; Th1: helper T-cell 1; Th17: helper T-cell 17; VICAM: vascular cell adhesion molecule 1; VLA4: very late antigen 4.
    Canakinumab, supplied by Novartis, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/canakinumab/canakinumab/pmc12694644-76-0-9
    Average 86 stars, based on 1 article reviews
    canakinumab - by Bioz Stars, 2026-09
    86/100 stars
    		  Buy from Supplier

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    Blocking mechanisms of interleukin-17 signaling in immune diseases. The addition of IL-6 + TGF-β or IL-6 + IL-1β + IL-23 to naïve mouse CD4 + T cells is required for T cells to upregulate RORγt and produce Th17 cytokines. IL-17 signaling can be achieved by blocking interleukin-17A (Secukinumab, Lxekizumab, and Nanakimab) and interleukin-17F (Bimekizumab) antibodies. IL-6 and TGF-β secreted by B cells are important inducers of Th17 cells. Antibodies targeting CD20 (Rituximab, Ofatumumab, Obinutuzumab, or Ocrelizumab) and CD19 (Inebilizumab) can lead to B-cell exhaustion and indirectly hinder the differentiation of Th17 cells. Inhibitors of IL-6R (Satralizumab), IL-1β (Canakinumab) or IL-23 (Uselkumab, Tildrakizumab, and Risankizumab), which indirectly target the IL-17 signaling pathway, can also affect Th17 cell differentiation. Blocking the infiltration of immune cells into the CNS can prevent autoimmune neuroinflammation. Natalizumab is an approved monoclonal antibody designed to specifically hinder this process by targeting VLA4/VCAM1, an integrin expressed on almost all immune cell subsets. DICAM and Integrin α3 are characteristically expressed on Th17 cells and bind to αvβ3 integrin and Laminin α5 on the blood‒brain barrier, respectively. Anti-DICAM and anti-αvβ3 integrin antibodies reduced the number of Th17 cells in the CNS. Created with BioRender.com. CD19: Cluster of differentiation 19; CD20: Cluster of differentiation 20; DICAM: dual immunoglobulin domain containing cell adhesion molecule; IL-1β: interleukin-1β; IL-6: interleukin-6; IL-17: interleukin-17; IL-17A: interleukin-17A; IL-17F: interleukin-17F; IL-17R: interleukin-17 receptor; IL-23: interleukin-23; TGF-β: tumor growth factor-β; Th0: helper T-cell 0; Th1: helper T-cell 1; Th17: helper T-cell 17; VICAM: vascular cell adhesion molecule 1; VLA4: very late antigen 4.

    Journal: Neural Regeneration Research

    Article Title: Interleukin-17 family in health and immune diseases: From origin to clinical implications

    doi: 10.4103/NRR.NRR-D-25-00026

    Figure Lengend Snippet: Blocking mechanisms of interleukin-17 signaling in immune diseases. The addition of IL-6 + TGF-β or IL-6 + IL-1β + IL-23 to naïve mouse CD4 + T cells is required for T cells to upregulate RORγt and produce Th17 cytokines. IL-17 signaling can be achieved by blocking interleukin-17A (Secukinumab, Lxekizumab, and Nanakimab) and interleukin-17F (Bimekizumab) antibodies. IL-6 and TGF-β secreted by B cells are important inducers of Th17 cells. Antibodies targeting CD20 (Rituximab, Ofatumumab, Obinutuzumab, or Ocrelizumab) and CD19 (Inebilizumab) can lead to B-cell exhaustion and indirectly hinder the differentiation of Th17 cells. Inhibitors of IL-6R (Satralizumab), IL-1β (Canakinumab) or IL-23 (Uselkumab, Tildrakizumab, and Risankizumab), which indirectly target the IL-17 signaling pathway, can also affect Th17 cell differentiation. Blocking the infiltration of immune cells into the CNS can prevent autoimmune neuroinflammation. Natalizumab is an approved monoclonal antibody designed to specifically hinder this process by targeting VLA4/VCAM1, an integrin expressed on almost all immune cell subsets. DICAM and Integrin α3 are characteristically expressed on Th17 cells and bind to αvβ3 integrin and Laminin α5 on the blood‒brain barrier, respectively. Anti-DICAM and anti-αvβ3 integrin antibodies reduced the number of Th17 cells in the CNS. Created with BioRender.com. CD19: Cluster of differentiation 19; CD20: Cluster of differentiation 20; DICAM: dual immunoglobulin domain containing cell adhesion molecule; IL-1β: interleukin-1β; IL-6: interleukin-6; IL-17: interleukin-17; IL-17A: interleukin-17A; IL-17F: interleukin-17F; IL-17R: interleukin-17 receptor; IL-23: interleukin-23; TGF-β: tumor growth factor-β; Th0: helper T-cell 0; Th1: helper T-cell 1; Th17: helper T-cell 17; VICAM: vascular cell adhesion molecule 1; VLA4: very late antigen 4.

    Article Snippet: Canakinumab , IL-1β , May. 2019, FDA approved , Novartis , SJIA, CAPS.

    Techniques: Blocking Assay, Cell Differentiation